General anesthesia stages and monitoring US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for General anesthesia stages and monitoring. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
General anesthesia stages and monitoring US Medical PG Question 1: A 59-year-old female presents to the emergency department after a fall. She reports severe pain in her right hip and an inability to move her right leg. Her past medical history is notable for osteoporosis, rheumatoid arthritis, and has never undergone surgery before. The patient was adopted, and her family history is unknown. She has never smoked and drinks alcohol socially. Her temperature is 98.8°F (37.1°C), blood pressure is 150/90 mmHg, pulse is 110/min, and respirations are 22/min. Her right leg is shortened, abducted, and externally rotated. A radiograph demonstrates a displaced femoral neck fracture. She is admitted and eventually brought to the operating room to undergo right hip arthroplasty. While undergoing induction anesthesia with inhaled sevoflurane, she develops severe muscle contractions. Her temperature is 103.4°F (39.7°C). A medication with which of the following mechanisms of action is indicated in the acute management of this patient’s condition?
- A. Ryanodine receptor antagonist (Correct Answer)
- B. Acetylcholine receptor agonist
- C. Serotonin 1B/1D agonist
- D. NMDA receptor antagonist
- E. GABA agonist
General anesthesia stages and monitoring Explanation: ***Ryanodine receptor antagonist***
- The patient's presentation with **high fever**, **muscle rigidity**, and **tachycardia** shortly after induction with **sevoflurane** is highly suggestive of **malignant hyperthermia (MH)**.
- **Dantrolene**, a **ryanodine receptor antagonist**, is the specific treatment for MH, as it blocks the excessive release of **calcium** from the sarcoplasmic reticulum in muscle cells.
*Acetylcholine receptor agonist*
- **Acetylcholine receptor agonists** (e.g., succinylcholine) stimulate muscle contraction and would worsen the muscle rigidity seen in malignant hyperthermia.
- These agents are often triggers for malignant hyperthermia when combined with volatile anesthetics.
*Serotonin 1B/1D agonist*
- **Serotonin 1B/1D agonists** (e.g., triptans) are primarily used in the acute treatment of migraines.
- They have no role in the management of malignant hyperthermia and would not address the underlying pathophysiology.
*NMDA receptor antagonist*
- **NMDA receptor antagonists** (e.g., ketamine) are dissociative anesthetics and analgesics.
- They do not directly affect the calcium release channels in skeletal muscle responsible for malignant hyperthermia.
*GABA agonist*
- **GABA agonists** (e.g., benzodiazepines, propofol) are central nervous system depressants used for sedation and anesthesia.
- While they can have muscle relaxant properties, they do not specifically target the **ryanodine receptor** pathway involved in malignant hyperthermia.
General anesthesia stages and monitoring US Medical PG Question 2: During a clinical study examining the diffusion of gas between the alveolar compartment and the pulmonary capillary blood, men between the ages of 20 and 50 years are evaluated while they hold a sitting position. After inhaling a water-soluble gas that rapidly combines with hemoglobin, the concentration of the gas in the participant's exhaled air is measured and the diffusion capacity is calculated. Assuming that the concentration of the inhaled gas remains the same, which of the following is most likely to increase the flow of the gas across the alveolar membrane?
- A. Deep exhalation
- B. Entering a cold chamber
- C. Treadmill exercise (Correct Answer)
- D. Standing straight
- E. Assuming a hunched position
General anesthesia stages and monitoring Explanation: ***Correct: Treadmill exercise***
- **Treadmill exercise** increases cardiac output and pulmonary blood flow, which in turn recruits and distends more **pulmonary capillaries**. This increases the **surface area** available for gas exchange and reduces the diffusion distance, thereby enhancing the flow of gas across the alveolar membrane.
- Exercise also typically leads to deeper and more frequent breaths, increasing the **ventilation-perfusion matching** and overall efficiency of gas exchange.
- According to Fick's law of diffusion (Vgas = A/T × D × ΔP), increasing the surface area (A) directly increases gas flow.
*Incorrect: Deep exhalation*
- **Deep exhalation** would empty the lungs more completely, potentially leading to alveolar collapse in some regions and thus **decreasing the alveolar surface area** available for gas exchange.
- This would also reduce the **driving pressure** for gas diffusion by lowering the alveolar concentration of the inhaled gas.
*Incorrect: Entering a cold chamber*
- Exposure to a **cold chamber** can cause **bronchoconstriction** in some individuals, particularly those with reactive airways, which would increase airway resistance and potentially reduce alveolar ventilation.
- While metabolic rate may slightly increase in the cold, the primary effect on the lungs is unlikely to promote increased gas diffusion in a healthy individual.
*Incorrect: Standing straight*
- **Standing straight** is a normal physiological posture and does not significantly alter the **pulmonary capillary recruitment** or the alveolar surface area in a way that would dramatically increase gas flow compared to a seated position.
- There might be minor gravitational effects on blood flow distribution, but these are generally less impactful than dynamic changes like exercise.
*Incorrect: Assuming a hunched position*
- **Assuming a hunched position** can restrict chest wall expansion and diaphragm movement, leading to **reduced tidal volume** and overall alveolar ventilation.
- This posture, by reducing lung volumes and potentially compressing the lungs, would likely **decrease the effective surface area** for gas exchange and therefore reduce gas flow.
General anesthesia stages and monitoring US Medical PG Question 3: A 17-year-old male presents with altered mental status. He was recently admitted to the hospital due to a tibial fracture suffered while playing soccer. His nurse states that he is difficult to arouse. His temperature is 98.6 deg F (37 deg C), blood pressure is 130/80 mm Hg, pulse is 60/min, and respirations are 6/min. Exam is notable for pinpoint pupils and significant lethargy. Which of the following describes the mechanism of action of the drug likely causing this patient's altered mental status?
- A. Neuronal hyperpolarization due to sodium influx
- B. Neuronal depolarization due to sodium efflux
- C. Neuronal depolarization due to potassium influx
- D. Neuronal hyperpolarization due to potassium efflux (Correct Answer)
- E. Neuronal hyperpolarization due to chloride influx
General anesthesia stages and monitoring Explanation: ***Neuronal hyperpolarization due to potassium efflux***
- The patient's symptoms of **altered mental status**, **pinpoint pupils**, and **respiratory depression** are classic for **opioid overdose**.
- Opioids act by binding to opioid receptors (mu, delta, kappa), which are **G-protein coupled receptors**. Activation of these receptors leads to **potassium efflux** and **calcium influx inhibition**, causing neuronal hyperpolarization and reduced neuronal excitability.
*Neuronal hyperpolarization due to sodium influx*
- **Sodium influx** typically causes depolarization, not hyperpolarization, making this option inconsistent with the mechanism of inducing neuronal inhibition.
- Hyperpolarization usually involves outward positive current (like potassium efflux) or inward negative current (like chloride influx).
*Neuronal depolarization due to sodium efflux*
- **Sodium efflux** (e.g., via the Na+/K+-ATPase) is crucial for maintaining resting membrane potential, but it does not directly lead to depolarization as described here.
- Depolarization is commonly associated with **sodium influx**, not efflux, causing the membrane potential to become more positive.
*Neuronal depolarization due to potassium influx*
- **Potassium influx** would make the cell less negative inside (depolarization), but this is not the primary mechanism of action for opioids.
- Opioids primarily cause **hyperpolarization** and reduced excitability, making this mechanism incorrect for the observed clinical picture caused by opioid overdose.
*Neuronal hyperpolarization due to chloride influx*
- While **chloride influx** does cause neuronal hyperpolarization (e.g., via GABA-A receptor activation by benzodiazepines), this is the mechanism for **GABAergic drugs**, not opioids.
- Opioids primarily achieve hyperpolarization through **potassium efflux**.
General anesthesia stages and monitoring US Medical PG Question 4: Two-hours into recovery from general anesthesia for an orthopedic fracture, a 34-year-old woman develops fever and masseter muscle rigidity with lockjaw. She has no history of a similar episode. She has no history of serious illness and takes no medications. She appears confused. In the recovery room, her blood pressure is 78/50 mm Hg, the pulse is 128/min, the respirations are 42/min, and the temperature is 40.3°C (104.5°F). Cardiopulmonary examination shows no abnormalities. Laboratory studies show:
Serum
Na+ 145 mEq/L
K+ 6.5 mEq/L
Arterial blood gas on room air
pH 7.01
PCO2 78 mm Hg
HCO3− 14 mEq/L
PO2 55 mm Hg
The patient is reintubated. Which of the following is the most appropriate next step in pharmacotherapy?
- A. Lorazepam
- B. Diphenhydramine
- C. Dantrolene (Correct Answer)
- D. Labetalol
- E. Cyproheptadine
General anesthesia stages and monitoring Explanation: ***Dantrolene***
- The patient exhibits classic signs of **malignant hyperthermia**, including
**masseter muscle rigidity**, **fever (40.3°C)**, **tachycardia (128/min)**,
**tachypnea (42/min)**, and **hypotension (78/50 mm Hg)**. The **elevated potassium (6.5
mEq/L)**, **acidosis (pH 7.01)**, and **hypercapnia (PCO2 78 mm Hg)**
further support this diagnosis.
- **Dantrolene** is the only specific antidote for malignant hyperthermia as
it acts as a **ryanodine receptor antagonist**, inhibiting calcium release
from the sarcoplasmic reticulum and thereby reducing muscle contracture and
heat production.
*Lorazepam*
- **Lorazepam** is a benzodiazepine used for treating seizures, anxiety, and
agitation, but it does **not address the underlying pathophysiology of
malignant hyperthermia**.
- While the patient appears confused, this is likely secondary to the
metabolic derangements and hyperthermia, not a primary indication for
lorazepam.
*Diphenhydramine*
- **Diphenhydramine** is an antihistamine used to treat allergic reactions or
sedation; it has no role in the management of malignant hyperthermia.
- It would not alleviate the muscle rigidity, hyperthermia, or metabolic
abnormalities seen in this patient.
*Labetalol*
- **Labetalol** is a beta-blocker used to manage hypertension and tachycardia,
but these are symptoms of malignant hyperthermia rather than the root
cause.
- While it could temporarily lower heart rate and blood pressure, it **does
not address the excessive calcium release** in skeletal muscle, which is
the hallmark of malignant hyperthermia.
*Cyproheptadine*
- **Cyproheptadine** is a serotonin antagonist used in the treatment of
serotonin syndrome.
- Malignant hyperthermia and serotonin syndrome share some clinical features
like hyperthermia, but the **trigger (anesthetic agents)** and underlying
mechanisms are different, making cyproheptadine ineffective here.
General anesthesia stages and monitoring US Medical PG Question 5: A 38-year-old man presents with sudden onset abdominal pain and undergoes an emergent laparoscopic appendectomy. The procedure is performed quickly, without any complications, and the patient is transferred to the post-operative care unit. A little while later, the patient complains of seeing people in his room and hearing voices talking to him. The patient has no prior medical or psychiatric history and does not take any regular medications. What is the mechanism of action of the anesthetic most likely responsible for this patient’s symptoms?
- A. Stimulation of μ-opioid receptors
- B. N-methyl-D-aspartate receptor antagonism (Correct Answer)
- C. Increased duration of GABA-gated chloride channel opening
- D. Blocking the fast voltage-gated Na+ channels
- E. Increased frequency of GABA-gated chloride channel opening
General anesthesia stages and monitoring Explanation: ***N-methyl-D-aspartate receptor antagonism***
- The patient's symptoms of **hallucinations** and **auditory phenomena** post-anesthesia are characteristic of **emergence delirium**, often associated with **ketamine**.
- Ketamine acts primarily as an **NMDA receptor antagonist**, which can lead to dissociative anesthesia and psychomimetic effects upon emergence.
*Stimulation of μ-opioid receptors*
- Opioids primarily cause **analgesia**, respiratory depression, and sedation by stimulating **μ-opioid receptors**.
- While opioids can cause some central nervous system effects like confusion or nightmares, the severe **hallucinations** described are not typical for this mechanism.
*Increased duration of GABA-gated chloride channel opening*
- This mechanism describes the action of **benzodiazepines** which potentiate GABAergic neurotransmission by increasing the **frequency** of chloride channel opening, while **barbiturates** increase the **duration**.
- These drugs typically cause **sedation** and **anxiolysis**, not acute psychosis or vivid hallucinations upon emergence.
*Blocking the fast voltage-gated Na+ channels*
- This is the primary mechanism of action for **local anesthetics** and certain **antiarrhythmic drugs**, leading to inhibition of nerve impulse conduction.
- While some systemic toxicity can occur with local anesthetics, it typically manifests as **seizures** or cardiovascular collapse, not dissociative emergence phenomena.
*Increased frequency of GABA-gated chloride channel opening*
- This is the mechanism of action for **benzodiazepines**, which enhance GABA's inhibitory effects by increasing the **frequency** of chloride channel opening.
- Similar to increased duration of opening, this leads to **sedation** and anxiolysis, not the vivid hallucinations seen in this patient.
General anesthesia stages and monitoring US Medical PG Question 6: A 27-year-old man presents to the emergency department after being hit by a car while riding his bike. The patient was brought in with his airway intact, vitals stable, and with a C-collar on. Physical exam is notable for bruising over the patient’s head and a confused man with a Glasgow coma scale of 11. It is noticed that the patient has a very irregular pattern of breathing. Repeat vitals demonstrate his temperature is 97.5°F (36.4°C), blood pressure is 172/102 mmHg, pulse is 55/min, respirations are 22/min and irregular, and oxygen saturation is 94% on room air. Which of the following interventions are most likely to improve this patient's vital signs?
- A. Head elevation, sedation, hypertonic saline, hypoventilation
- B. Lower head, sedation, hypertonic saline, hypoventilation
- C. Head elevation, sedation, mannitol, hyperventilation (Correct Answer)
- D. Head elevation, norepinephrine, mannitol, hyperventilation
- E. Lower head, sedation, hypertonic saline, hyperventilation
General anesthesia stages and monitoring Explanation: ***Head elevation, sedation, mannitol, hyperventilation***
- This patient presents with signs of **increased intracranial pressure (ICP)**, indicated by **Cushing's triad** (hypertension, bradycardia, irregular respirations) and a decreased Glasgow Coma Scale (GCS) after head trauma. **Head elevation** to 30 degrees promotes venous outflow from the brain, reducing ICP.
- **Sedation** lowers metabolic demand and reduces agitation, which can otherwise increase ICP. **Mannitol** is an osmotic diuretic that rapidly draws fluid from the brain, decreasing cerebral edema. **Hyperventilation** temporarily reduces ICP by causing cerebral vasoconstriction through decreased pCO2.
*Head elevation, sedation, hypertonic saline, hypoventilation*
- While **head elevation**, **sedation**, and **hypertonic saline** (an alternative osmotic agent to mannitol) are appropriate for ICP management, **hypoventilation** would increase pCO2, causing cerebral vasodilation and worsening ICP.
- The combination of effective and ineffective ICP-reducing strategies makes this an incorrect option.
*Lower head, sedation, hypertonic saline, hypoventilation*
- **Lowering the head** would impede venous drainage from the brain and increase ICP, which is detrimental in this scenario.
- As mentioned, **hypoventilation** is contraindicated as it exacerbates cerebral edema and elevated ICP.
*Head elevation, norepinephrine, mannitol, hyperventilation*
- While **head elevation**, **mannitol**, and **hyperventilation** are appropriate, **norepinephrine** is primarily used to treat hypotension and maintain cerebral perfusion pressure (CPP) if blood pressure is dangerously low.
- In this case, the patient is hypertensive (**blood pressure 172/102 mmHg**), so norepinephrine would further increase blood pressure and ICP.
*Lower head, sedation, hypertonic saline, hyperventilation*
- **Lowering the head** is contraindicated as it directly increases ICP by hindering venous outflow from the brain.
- Although **sedation**, **hypertonic saline**, and **hyperventilation** are useful for ICP control, the incorrect positioning makes this option less suitable.
General anesthesia stages and monitoring US Medical PG Question 7: A 22-year-old man is brought to the emergency department 10 minutes after falling down a flight of stairs. An x-ray of the right wrist shows a distal radius fracture. A rapidly acting intravenous anesthetic agent is administered, and closed reduction of the fracture is performed. Following the procedure, the patient reports palpitations and says that he experienced an “extremely vivid dream,” in which he felt disconnected from himself and his surroundings while under anesthesia. His pulse is 110/min and blood pressure is 140/90 mm Hg. The patient was most likely administered a drug that predominantly blocks the effects of which of the following neurotransmitters?
- A. Endorphin
- B. Dopamine
- C. Norepinephrine
- D. Glutamate (Correct Answer)
- E. Gamma-aminobutyric acid
General anesthesia stages and monitoring Explanation: ***Glutamate***
- The patient's symptoms of **dissociative anesthesia**, **vivid dreams**, and **palpitations** are characteristic of **ketamine**, which is a rapidly acting intravenous anesthetic.
- Ketamine works primarily as a **non-competitive antagonist of the NMDA receptor**, blocking the excitatory effects of glutamate.
*Endorphin*
- Endorphins are **endogenous opioid peptides** that act on opioid receptors, producing analgesia and euphoria.
- Drugs acting predominantly on endorphin pathways (e.g., opioids) do not typically cause dissociative states or vivid dreams as described.
*Dopamine*
- Dopamine is involved in reward, motivation, and motor control; drugs affecting dopamine (e.g., antipsychotics, Parkinson's medications) have different primary effects.
- Blocking dopamine would not directly produce dissociative anesthesia or the cardiovascular and hallucinatory side effects seen with ketamine.
*Norepinephrine*
- Norepinephrine is a neurotransmitter involved in the **sympathetic nervous system** and its effects on alertness, vigilance, and the fight-or-flight response.
- While ketamine can cause sympathetic stimulation leading to increased heart rate and blood pressure, its primary mechanism of anesthesia is not through norepinephrine blockade.
*Gamma-aminobutyric acid*
- **Gamma-aminobutyric acid (GABA)** is the main inhibitory neurotransmitter in the CNS, and drugs that enhance GABAergic activity (e.g., benzodiazepines, propofol) typically cause sedation, anxiolysis, and amnesia.
- This patient's symptoms of vivid dreams and dissociation are opposite to the effects of GABAergic anesthetics, which often produce unconsciousness without such mental experiences.
General anesthesia stages and monitoring US Medical PG Question 8: A 42-year-old man presents to his family physician for evaluation of oral pain. He states that he has increasing pain in a molar on the top left of his mouth. The pain started 1 week ago and has been progressively worsening since then. His medical history is significant for hypertension and type 2 diabetes mellitus, both of which are currently controlled with lifestyle modifications. His blood pressure is 124/86 mm Hg, heart rate is 86/min, and respiratory rate is 14/min. Physical examination is notable for a yellow-black discoloration of the second molar on his left upper mouth. The decision is made to refer him to a dentist for further management of this cavity. The patient has never had any dental procedures and is nervous about what type of sedation will be used. Which of the following forms of anesthesia utilizes solely an oral or intravenous anti-anxiety medication?
- A. Minimal Sedation (Correct Answer)
- B. Dissociation
- C. Regional anesthesia
- D. Epidural anesthesia
- E. Deep sedation
General anesthesia stages and monitoring Explanation: ***Minimal Sedation***
- This involves using **oral** or **intravenous anti-anxiety medications** to help a patient relax while remaining conscious and responsive.
- The patient can still respond to verbal commands but is in a state of decreased anxiety and awareness.
*Dissociation*
- This is a state induced by certain drugs, like **ketamine**, where the patient feels detached from their body and environment.
- While it can be achieved intravenously, it is not solely an anti-anxiety medication effect and involves a different neurological state.
*Regional anesthesia*
- This involves injecting a **local anesthetic** near nerves to numb a specific part of the body, such as a limb or a jaw section for dental procedures.
- It primarily provides pain relief by blocking nerve signals and does not typically involve anti-anxiety medication as its sole component for sedation.
*Epidural anesthesia*
- This form of regional anesthesia involves injecting a **local anesthetic** into the **epidural space** surrounding the spinal cord to block pain signals.
- It is used for pain control during surgery or childbirth and does not involve oral or intravenous anti-anxiety medication as the primary method of sedation.
*Deep sedation*
- This involves a more profound depression of consciousness than minimal sedation, where the patient may be difficult to arouse but still responds purposefully to repeated or painful stimulation.
- While it can use intravenous medications, it typically involves a combination of sedatives and analgesics to achieve a deeper state of unresponsiveness, beyond just anti-anxiety medication.
General anesthesia stages and monitoring US Medical PG Question 9: A 28-year-old male presents to his primary care physician with complaints of intermittent abdominal pain and alternating bouts of constipation and diarrhea. His medical chart is not significant for any past medical problems or prior surgeries. He is not prescribed any current medications. Which of the following questions would be the most useful next question in eliciting further history from this patient?
- A. "Does the diarrhea typically precede the constipation, or vice-versa?"
- B. "Is the diarrhea foul-smelling?"
- C. "Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life"
- D. "Are the symptoms worse in the morning or at night?"
- E. "Can you tell me more about the symptoms you have been experiencing?" (Correct Answer)
General anesthesia stages and monitoring Explanation: ***Can you tell me more about the symptoms you have been experiencing?***
- This **open-ended question** encourages the patient to provide a **comprehensive narrative** of their symptoms, including details about onset, frequency, duration, alleviating/aggravating factors, and associated symptoms, which is crucial for diagnosis.
- In a patient presenting with vague, intermittent symptoms like alternating constipation and diarrhea, allowing them to elaborate freely can reveal important clues that might not be captured by more targeted questions.
*Does the diarrhea typically precede the constipation, or vice-versa?*
- While knowing the sequence of symptoms can be helpful in understanding the **pattern of bowel dysfunction**, it is a very specific question that might overlook other important aspects of the patient's experience.
- It prematurely narrows the focus without first obtaining a broad understanding of the patient's overall symptomatic picture.
*Is the diarrhea foul-smelling?*
- Foul-smelling diarrhea can indicate **malabsorption** or **bacterial overgrowth**, which are important to consider in some gastrointestinal conditions.
- However, this is a **specific symptom inquiry** that should follow a more general exploration of the patient's symptoms, as it may not be relevant if other crucial details are missed.
*Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life*
- Quantifying pain intensity is useful for assessing the **severity of discomfort** and monitoring changes over time.
- However, for a patient with intermittent rather than acute, severe pain, understanding the **character, location, and triggers** of the pain is often more diagnostically valuable than just a numerical rating initially.
*Are the symptoms worse in the morning or at night?*
- Diurnal variation can be relevant in certain conditions, such as inflammatory bowel diseases where nocturnal symptoms might be more concerning, or functional disorders whose symptoms might be stress-related.
- This is another **specific question** that should come after gathering a more complete initial picture of the patient's symptoms to ensure no key information is overlooked.
General anesthesia stages and monitoring US Medical PG Question 10: You are a resident on an anesthesiology service and are considering using nitrous oxide to assist in placing a laryngeal mask airway (LMA) in your patient, who is about to undergo a minor surgical procedure. You remember that nitrous oxide has a very high minimal alveolar concentration (MAC) compared to other anesthetics. This means that nitrous oxide has:
- A. no effect on lipid solubility or potency
- B. decreased lipid solubility and decreased potency (Correct Answer)
- C. decreased lipid solubility and increased potency
- D. increased lipid solubility and increased potency
- E. increased lipid solubility and decreased potency
General anesthesia stages and monitoring Explanation: ***Decreased lipid solubility and decreased potency***
- A **very high MAC** indicates that a large concentration of the anesthetic agent is required to produce immobility in 50% of patients, signifying **low potency**.
- According to the **Meyer-Overton rule**, anesthetic potency is directly correlated with lipid solubility; therefore, low potency implies **decreased lipid solubility**.
*No effect on lipid solubility or potency*
- This statement is incorrect as MAC is a direct measure of potency, and potency is linked to lipid solubility by the **Meyer-Overton rule**.
- A high MAC unequivocally indicates **low potency**, and indirectly, low lipid solubility.
*Decreased lipid solubility and increased potency*
- This is incorrect because **increased potency** would be associated with a **low MAC**.
- Potency and lipid solubility are positively correlated, so decreased lipid solubility would lead to **decreased potency**.
*Increased lipid solubility and increased potency*
- This is incorrect; while **increased lipid solubility** is associated with **increased potency**, increased potency would manifest as a **low MAC**, not a high one.
- The given information states a **very high MAC**, which signifies low potency.
*Increased lipid solubility and decreased potency*
- This statement contradicts the **Meyer-Overton rule**, which establishes a direct relationship between lipid solubility and anesthetic potency.
- Therefore, **increased lipid solubility** should correspond to **increased potency**, not decreased potency.
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